Rabbit NFkB p50 Polyclonal Antibody | anti-NFkB p50 antibody

NFkB p50 (C20) Antibody

Cat. Num. AAA440032

• Reactivity: Mouse, rat, human
• Applications: Western Blot, Immunoprecipitation, Immunohistochemistry
• Synonyms: NFkB p50; Polyclonal Antibody; NFkB p50 (C20) Antibody; anti-NFkB p50 antibody

• Host: Rabbit
• Reactivity: Mouse, rat, human
• Clonality: Polyclonal
• Specificity: Mouse, rat and human NFkB p50 and p105
• Form/Format: 200 ug/ml rabbit polyclonal IgG in 1 ml PBS containing 0.1 % sodium azide and 0.2% gelatin.
• Concentration: 0.200 mg/ml (varies by lot)

• Applicable Applications for anti-NFkB p50 antibody: Western Blot (WB), Immunoprecipitation (IP), Immunohistochemistry (IHC)
• Application Notes: NFkB p50 (C20) DB035 reacts with NFkB p50 and p105 of mouse, rat, and human origin by western blotting, immunoprecipitation and immunohistochemistry. Western blotting starting dilution: 1:400.
• Origin: NFkB p50 is provided as an affinity purified rabbit polyclonal antibody, raised against a peptide mapping to the carboxy terminus of human NFkB p50.
• Immunogen: Synthetic peptide mapping to the carboxy terminal domain of human NFkB p50.
• Preparation and Storage: Store this product at 4 degree C, do not freeze. The product is stable for one year from the date of shipment.

Western Blot (WB)

Related Product Information for anti-NFkB p50 antibody

Members of the rel/NFkB family of transcription factors are involved in the regulation of cellular responses, such as growth, development, and the inflammatory response. They share a structural motif known as the rel homology region (RHR), the C-terminal one third of which mediates protein dimerization (2, 6, 8). Complexes of p50 (NF-kB1) or p52 (NF-kB2) are generated through the processing of p105 and p100 precursors, respectively. These are usually associated with members of the Rel family (p65, c-Rel, Rel B). The homo- and heterodimer formed through combinations of NFkB/Rel proteins bind distinct kB sites to regulate the transcription of different genes (7, 9). In resting cells, NFkB is retained in the cytoplasm bound to inhibitory proteins of the IkB family. Degradation of IkB proteins occurs with cell activation, via of variety of signals, including inflammatory cytokines and bacterial lipopolysaccharides (LPS) as well as oxidative and fluid mechanical stress. This results in nuclear translocation of NFkB and the transcriptional gene activation of proinflammatory genes (1, 9). It has been suggested that NFkB plays a role in the development of numerous pathological states. Activation of NFkB induces gene programs leading to transcription of factors that promote inflammation, such as leukocyte adhesion molecules, cytokines, and chemokines. It is also thought that there are some substances with possible anti-inflammatory effects that are also NFkB regulated. There is some evidence indicating NFkB as a key factor in the pathophysiology of cardiac ischemia-reperfusion injury as well as the development of insulin dependent Diabetes Mellitus (4, 3).

References

1.) Leitch D, Barrans SL, Jack AS, Owen RG. 2003. Dysregulation of apoptosis in Waldenstrom's macroglobulinemia does not involve nuclear factor kappa B activation. Semin Oncol. Apr;30(2):161-4.2.) Cho J and Tsichlis PN. 2005. Phosphorylation at Thr-290 regulates Tpl2 binding to NF-{kappa}B1/p105 and Tpl2 activation and degradation by lipopolysaccharide. Proc Natl Acad Sci U S A. Feb 15;102(7):2350-5. 3.) Cho J, Melnick M, Solidakis GP, Tsichlis PN. Tpl2 (Tumor Progression Locus 2) Phosphorylation at Thr290 Is Induced by Lipopolysaccharide via an I{kappa}-B Kinase-{beta}-dependent Pathway and Is Required for Tpl2 Activation by External Signals.J Biol Chem. 2005 May 27;280(21):20442-8. 4.) Joo SS, Won TJ, Lee do I. Potential role of ursodeoxycholic acid in suppression of nuclear factor kappa B in microglial cell line (BV-2). Arch Pharm Res. 2004 Sep;27(9):954-60. 5.) Das S, Cho J, Lambertz I, Kelliher MA, Eliopoulos AG, Du K, Tsichlis PN. Tpl2/Cot Signals Activate ERK, JNK, and NF-{kappa}B in a Cell-type and Stimulus-specific Manner. J Biol Chem. 2005 Jun 24;280(25):23748-57.6.) Pelletier M, Girard D. 2006. Differential effects of IL-15 and IL-21 in myeloid (CD11b+) and lymphoid (CD11b-) bone marrow cells. J Immunol. Jul 1;177(1):100-8.7.) Snyder AR, Morgan WF. 2005. Lack of consensus gene expression changes associated with radiation-induced chromosomal instability. DNA Repair (Amst). Aug 15;4(9):958-70.8.) Kang HB, Kim YE, Kwon HJ, Sok DE, Lee Y. 2007. Enhancement of NF-kappaB expression and activity upon differentiation of human embryonic stem cell line SNUhES3. Stem Cells Dev. 2007 Aug;16(4):615-23.

1. Lentsch AB, Ward PA. The NFkB/IkappaB system in acute inflammation. Arch Immunol Ther Exp (Warsz). 48(2): 59-63. 2. Hatada EN, Krappmann D, Scheidereit C. NF-kappaB and the innate immune response. Curr Opin Immunol. 2000 Feb; 12(1): 52-8 3. Ho E, Bray TM. Antioxidants, NFkappaB activation, and diabetogenesis. Proc Soc Exp Biol Med. 1999 Dec; 222(3): 205-13.4. Valen G, Yan ZQ, Hansson GK. Nuclear factor kappa-B and the heart. J Am Coll Cardiol. 2001 Aug; 38(2): 307-14.5. Chen FE, Kempiak S, Huang DB, Phelps C, Ghosh G. Construction, expression, purification and functional analysis of recombinant NFkappaB p50/p65 heterodimer. Protein Eng. 1999 May; 12(5): 423-8.6. Sengchanthalangsy LL, Datta S, Huang DB, Anderson E, Braswell EH, Ghosh G. Characterization of the dimer interface of transcription factor NFkappaB p50 homodimer. J Mol Biol. 1999 Jun 18; 289(4): 1029-40.7. Huang DB, Huxford T, Chen YQ, Ghosh G. The role of DNA in the mechanism of NFkappaB dimer formation: crystal structures of the dimerization domains of the p50 and p65 subunits. Structure. 1997 Nov 15; 5(11): 1427-36.8. Magnani M, Crinelli R, Bianchi M, Antonelli A. The ubiquitin-dependent proteolytic system and other potential targets for the modulation of nuclear factor-kB (NF-kB). Curr Drug Targets. 2000 Dec; 1(4): 387-99.